Bowel ischaemia-reperfusion-induced liver and lung injury: The fundamental role of eicosanoids and xanthine oxidase-generated oxygen free radicals

A. A. Weinbroum*, G. Coldman, Y. Kluger, M. Hag, S. Marmour, P. Sorkine, J. M. Klausner, D. Niv, V. Rudick

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Objective: To assess complementary induction of remote organ injury following bowel ischaemia-reperfusion by eicosanoids and xanthine oxidase. Design: Randomized, controlled, animal study. Setting: Hospital-based animal research facility. Materials: 40 rats in 5 groups. Interventions: Sham laparotomy, laparotomy and superior mesenteric artery occlusion (ischaemia 1h) and reperfusion (3h) or laparotomy and arterial occlusion and reperfusion in rats treated with thromboxane synthase inhibitor OKY-046, leukotrienes synthase inhibitor diethylcarbamazine or xanthine oxidase inhibitor allopurinol. Main outcome measures: Bowel, liver and lung wet: dry weight ratio, tissue: circulation albumin I125 permeability index, polymorphonuclear neutrophils tissue counts. Results: Ischaemia intestinal and lungs wet: dry ratios increased by 50% over sham or treatment groups; liver ratios were similar. Albumin indexes in ischaemia organs were 1.5-3 times more than shams and treatment values, and allopurinol normalized it best. Neutrophils counts in all ischaemia organs were double that of shams; allopurinol prevented sequestration completely, eicosanoids inhibitors did so partially. Conclusions: Xanthine oxidase initiated remote organ injury following bowel ischaemia-reperfusion. Allopurinol prevented it entirely while eicosanoids inhibitors only partially.

Original languageEnglish
Pages (from-to)624-630
Number of pages7
JournalMedical Science Monitor
Volume3
Issue number5
StatePublished - 1997
Externally publishedYes

Keywords

  • Bowel
  • Ischaemia-reperfusion
  • Leukotriene
  • Oxygen free radicals
  • Remote organ injury
  • Thromboxane
  • Xanthine oxidase

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